The mu opioid receptor is a member of G-protein coupled receptor super family. We have proposed that the mu receptor undergoes constitutive activation upon treatment with agonist, which may serve as a driving force underlying narcotic tolerance and dependence. Furthermore, phosphorylation of the mu receptor by a class of g-protein receptor kinase (GRK) is important for the formation of the constitutive mu receptor activation. Therefore, suitable GRK inhibitors can be useful for the prevention and treatment of narcotic tolerance and dependence. We have built a GRK2 (also known as beta adrenergic receptor kinase 1) model based on the homology to protein kinase A. Currently we are searching the chemical base for the inhibitors of this kinase model and information generated from the modeling is being tested in functional assay. Availability and usage of the Computer Graphics Laboratory is essential to this project. I greatly appreciated the support from the Computer Graphics Lab.